In lieu of an abstract, here is a brief excerpt of the content:

SEXIST DISEASES MICHEL GARENNE* and MONIQUE LAEONf Introduction In human populations, females usually have a lower mortality than males at any age. This pattern is observed for most causes of death due to chronic diseases, accidents, and violence [1-4]. However, lower female mortality is not universal, and a reverse pattern of excess female mortality has been observed for some infectious diseases. Whooping cough is often quoted in the medical literature as being more lethal for girls than for boys [5] . Another such recently documented disease is measles [6]. Both are airborne diseases for which the incidence is virtually identical for males and females. This implies that differences in mortality demonstrate a difference in case fatality. The excess female mortality from measles and whooping cough is found throughout the world, in places as different as Europe,Japan, North America, Africa, and Latin America. This implies a biological difference rather than a cultural pattern, and therefore a higher susceptibility for females . In casual reports made throughout the world, and especial!)' among older children and young adults, excess female mortality has been observed in certain other infectious diseases, such as tuberculosis, typhoid and paratyphoid , typhus, smallpox, scarlet fever, diphtheria, influenza, and congenital syphilis [7-9]. The two striking features of these early studies are the highly selective list of diseases exhibiting excess female mortality and the changing pattern by age. Late childhood and early adulthood appear to be the life periods when females are the most vulnerable compared to males. The explanation for a higher vulnerability of females for certain infectious diseases could be sought in differences between the male and female The authors would like to thank Prof. Samuel Preston (University of Pennsylvania) and Dr. Brian Ward (McGiIl University) for comments on the demographic and immunologic aspects of the manuscript; Dr. Desmond Martin (National Institute for Virology, South Africa) for personal communications on various diseases; and Ms. Shelah Bhalti (Harvard University) for editorial comments. * Centre Francais sur la Population et le Développement (CEPED), 15 rue de l'Ecole de Médecine, 75270 Paris Cedex 06, France. f Institut Pasteur, 25 rue du Docteur Roux, 75724 Paris Cedex 15, France.© 1998 by The University of Chicago. All rights reserved. 0031-5892/98/41 02-1049$01.00 176 Michel Garenne and Monique Lafon ¦ Sexist Diseases immune systems. Recently, lymphocytes have been divided into two subsets, Th-I and Th-2, according to the cytokines they produce [10, H]. Th-I are major producers of IL-2, and IFN-?, whereas Th-2 produce high levels of IL-4, IL-5, IL-6, and IL-IO. Stimulation of Th-2 lymphocytes activates antibody secretion, whereas stimulation of Th-I lymphocytes facilitates cytotoxic T cells. The balance between Th-I and Th-2 responses seems to be essential for resistance to disease and survival. Recently, evidence accumulated showing that male and female immune systems do not mount immune responses in the same way [12]. Females seem to favor a Th-2 response , whereas males favor a Th-I response. This is especially true during pregnancy, when there is a drop of Th-I cytokines and an increase of Th-2 cytokines [13, 14]. The fact that sex hormones can regulate the Th-I/ Th-2 balance [15, 16] could explain the differences between male and female mortality for certain infectious diseases, especially among young adults when the level of sex hormones is the highest. The goals of this study were (1) to systematically search for groups of infectious diseases showing different male and female mortality during late childhood and early adulthood, (2) to investigate the characteristics of the Th-I and Th-2 responses to certain infectious diseases, and (3) to test the plausibility of the sex hormones explanation. This hypothesis linking the hormonal and the immunological systems and the way the body copes with infectious diseases could explain both the direction and the changing pattern of gender differences in mortality by age. Demographic Evidence The demographic data originated from the World Health Statistics, a databank computerized by the World Health Organization from national causes of death statistics. Data originated from 110 countries throughout the world between 1950 and 1989. These were mostly developed...

pdf

Share